The proposed work includes the study of glucose metabolism and its role in various types of cataracts, e.g., human senile cataract and human diabetic cataract. Emphases are placed on the properties of the regulatory mechanisms in the metabolic pathways such as glycolysis, hexosemonophosphate shunt, glutathione redox, mitochondrial activity and the sorbitol pathway. We identify the weak links in these pathways that fail to protect the lens from oxidative and/or osmotic stresses. Prevention of cataractogenesis is possible when the stresses are removed or when the weak links are bypassed. One such example is the use of aldose reductase inhibitors to prevent human diabetic cataracts by eliminating osmotic stress caused by the accumulation of sorbitol.